- New research indicates that glaucoma drugs can prevent cognitive impairment linked to Alzheimer’s disease in mice.
- The drugs work by clearing amyloid beta from blood vessels, lowering inflammation, and improving cell function.
- Neuroscientists agree the results of the study are promising, however; further research is needed in humans.
One of the main warning signs of Alzheimer’s Disease (AD) is the accumulation of amyloid beta in the brain’s blood vessels. Amyloid beta is a protein that contributes to plaque buildup, which can impact the amount of nutrients and oxygen the brain receives.
Ultimately, this can cause cerebral amyloid angiopathy (CAA), a leading cause of cognitive decline among older adults.
To explore this concept further, researchers at the Lewis Katz School of Medicine at Temple University investigated two FDA approved drugs to see if they mitigate the effects of CAA and cognitive decline in a model of Alzheimer’s.
They made an interesting discovery and found that glaucoma drugs prevent cognitive impairment linked to Alzheimer’s disease in mice.
The study was published in the journal
Researchers conducted this study with mice using carbonic anhydrase inhibitors (CAIs), which help treat other conditions including glaucoma and high-altitude sickness.
The drugs also help get rid of amyloid beta from blood vessels and glial cells, which ultimately helps prevent cognitive impairment, lowering inflammation and improving cell function.
Keiland Cooper, a doctoral researcher in cognitive science and neuroscience at the University of California, Irvine, explained to Medical News Today how amyloid beta affects the brain of a person with Alzheimer’s disease.
“Amyloid beta is a protein that is naturally produced in the brain. In the healthy brain, it is thought to play a role in neuronal development and synaptic plasticity,” said Cooper.
“However, in people with Alzheimer’s disease, amyloid beta can form plaques that build up between neurons. These plaques are one of the two classical hallmarks of the disease— plaques and tau tangles. These plaques are thought to damage the neurons and lead to cognitive decline,” he continued.
This relates to the “amyloid hypothesis,” which theorizes that amyloid beta is the main cause of Alzheimer’s disease.
“This theory is supported by the fact that people with Alzheimer’s disease have high levels of amyloid beta in their brains and that amyloid beta plaques can be found in the brains of people with Alzheimer’s disease even before they start to show symptoms,” Cooper said.
However, studies in recent years have discredited the amyloid hypothesis.
For example, Cooper explained that some studies have shown that people with Alzheimer’s disease can have low levels of amyloid beta and that some people with high levels of amyloid beta do not develop Alzheimer’s disease.
This suggests that amyloid beta may not be the only cause of Alzheimer’s disease and that other factors may also play a role.
This study may pave the way for a new way of thinking regarding treatment for AD.
“It’s good to see research focused not only on the typical amyloid pathology we think about in Alzheimer’s disease, but also on cerebral amyloid angiopathy (CAA),” Dr. Adam Mecca, Ph.D., assistant professor at the Yale School of Medicine and associate director of the Alzheimer’s Disease Research Unit at the Alzheimer’s Disease Research Center, told MNT.
“In CAA, we find deposits of amyloid in walls of small arteries within the brain that is associated with cerebrovascular disease,” he said.
Understanding more about CAA and how it affects the brains of Alzheimer’s patients may also be helpful.
“The article points out that up to 90 percent of people who have Alzheimer’s disease also have some degree of CAA. That’s consistent with what we see in our local center when we [examine] brain tissue from people who have been diagnosed with Alzheimer’s. The fact that CAA is so common makes me wonder about the role it plays in the Alzheimer’s disease process,” Dr. Mecca said.
Although research is still in its early stages, the findings remain promising.
“The authors have taken an efficient approach to repurpose drugs that have already been tested for safety and approved for another use. This can be a high-yield way to look for new therapies because they’ll spend less time in the development pathway,” said Dr. Mecca.
“The findings of this research are important first steps toward developing a new type of therapy for Alzheimer’s disease, but of course, we would need to test the effectiveness in humans.”
— Dr. Adam Mecca
One of the key takeaways from these findings is that CAIs can reduce aspects of Alzheimer’s pathology. This can point research regarding Alzheimer’s treatment and prevention in a new direction.
Additionally, “the class of drugs studied are Carbonic Anhydrase Inhibitors (CAIs). The results don’t provide a clear idea of why the CAIs would improve Alzheimer’s disease, but they do provide some evidence that the drugs may reduce various aspects of Alzheimer’s pathology,” Dr. Mecca noted.
“The authors point out that there is some evidence that the enzymes targeted by CAIs are upregulated in mouse models of Alzheimer’s, and maybe even in human disease, so there’s a sense that inhibiting it would be helpful. Overall, the results are encouraging and offer a novel approach to Alzheimer’s disease treatment,” he added.
While these study findings on mice are encouraging, it doesn’t necessarily mean the results will be repeated in human trials.
“Animal studies of drug effectiveness are a good first step toward developing Alzheimer’s disease treatments, but it’s important to note that many of the drugs that succeed at that phase will fail in human studies,” Dr. Mecca explained.
“These are important studies that can point us in the right direction and there’s a lot more work that needs to be done before you can imagine having a therapeutic agent we can use in humans,” he added.
Cooper agrees that rodent models can be a valuable tool for biomedical research.
“They can be used to study the mechanisms of disease, to test the safety and efficacy of new treatments, and to develop new therapeutic strategies,” said Cooper.
“However, it is important to remember that rodent models are not a perfect substitute for human clinical trials,” he added.
For example, mice do not get Alzheimer’s disease in the same way that humans do, instead, they are altered genetically to exhibit similar symptoms as humans.”
In short, further study is required.
“Further, there are different mouse models that exhibit different symptoms, and each can respond to treatments in different ways. A common phrase in the field is that ‘we have cured Alzheimer’s disease hundreds of times…in a mouse’. It is important to note that more research is needed to confirm these findings in humans,” Cooper said.